Evidence map›Paper›PMID 35594658›Full record

SynthesisEBioMedicine2022

Gut dysbiosis in rheumatic diseases: A systematic review and meta-analysis of 92 observational studies.

Yilun Wang, Jie Wei, Weiya Zhang, Michael Doherty, Yuqing Zhang, Haibin Xie, Wei Li, Ning Wang, Guanghua Lei, Chao Zeng

Open access · goldAbstract readMeta-AnalysisSystematic Review
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in EBioMedicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 9 pooled it
10.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

101 citing papers in PubMed, 9 syntheses or guidelines pooled it, 135 citations in OpenAlex.

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  11. Review
  12. Article
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  15. Intestinal microbiota and arthritis.EULAR rheumatology open · 2026
    Review
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  19. Review
  20. Nutrients · 2026
    Article

41 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 3 countries.

Yilun WangDepartment of Orthopaedics, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, Hunan 410008, China.
Jie WeiHealth Management Center, Xiangya Hospital, Central South University, Changsha, China; Hunan Key Laboratory of Joint Degeneration and Injury, Changsha, China.
Weiya ZhangUniversity of Nottingham, Nottingham, UK; Pain Centre Versus Arthritis UK, Nottingham, UK.
Michael DohertyUniversity of Nottingham, Nottingham, UK; Pain Centre Versus Arthritis UK, Nottingham, UK.
Yuqing ZhangDivision of Rheumatology, Allergy, and Immunology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, USA; The Mongan Institute, Massachusetts General Hospital, Harvard Medical School, Boston, USA.
Haibin XieDepartment of Orthopaedics, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, Hunan 410008, China.
Wei LiDepartment of Orthopaedics, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, Hunan 410008, China.
Ning WangDepartment of Orthopaedics, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, Hunan 410008, China.
Guanghua LeiDepartment of Orthopaedics, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, Hunan 410008, China; Hunan Key Laboratory of Joint Degeneration and Injury, Changsha, China; National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China. Electronic address: lei_guanghua@csu.edu.cn.
Chao ZengDepartment of Orthopaedics, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, Hunan 410008, China; Hunan Key Laboratory of Joint Degeneration and Injury, Changsha, China; National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China. Electronic address: zengchao@csu.edu.cn.
Central South University · CNUniversity of Nottingham · GBHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEmerging evidence suggests that dysbiosis in gut microbiota may contribute to the occurrence or development of several rheumatic diseases. Since gut microbiota dysbiosis is potentially modifiable, it has been postulated to be a promising preventive or therapeutic target for rheumatic diseases. However, the current understanding on the potential associations between gut microbiota and rheumatic diseases is still inadequate. Therefore, we aimed to synthesise the accumulating evidence for the relation of gut microbiota to rheumatic diseases.

methodsThe PubMed, Embase and Cochrane Library were searched from inception to March 11, 2022 to include observational studies evaluating the associations between gut microbiota and rheumatic diseases. Standardised mean difference (SMD) of α-diversity indices between rheumatic diseases and controls were estimated using random-effects model. β-diversity indices and relative abundance of gut microbes were summarised qualitatively.

findingsOf the included 92 studies (11,998 participants), 68 provided data for α-diversity. Taken together as a whole, decreases in α-diversity indices were consistently found in rheumatic diseases (observed species: SMD = -0.36, [95%CI = -0.63, -0.09]; Chao1: SMD = -0.57, [95%CI = -0.88, -0.26]; Shannon index: SMD = -0.33, [95%CI = -0.48, -0.17]; Simpson index: SMD = -0.32, [95%CI = -0.49, -0.14]). However, when specific rheumatic diseases were examined, decreases were only observed in rheumatoid arthritis (observed species: SMD = -0.51, [95%CI = -0.78, -0.24]; Shannon index: SMD = -0.31, [95%CI = -0.49, -0.13]; Simpson index: SMD = -0.31, [95%CI = -0.54, -0.08]), systemic lupus erythematosus (Chao1: SMD = -1.60, [95%CI = -2.54, -0.66]; Shannon index: SMD = -0.63, [95%CI = -1.08, -0.18]), gout (Simpson index: SMD = -0.64, [95%CI = -1.07, -0.22]) and fibromyalgia (Simpson index: SMD = -0.28, [95%CI = -0.44, -0.11]), whereas an increase was observed in systemic sclerosis (Shannon index: SMD = 1.25, [95%CI = 0.09, 2.41]). Differences with statistical significance in β-diversity were consistently reported in ankylosing spondylitis and IgG4-related diseases. Although little evidence of disease specificity of gut microbes was found, shared alterations of the depletion of anti-inflammatory butyrate-producing microbe (i.e., Faecalibacterium) and the enrichment of pro-inflammatory microbe (i.e., Streptococcus) were observed in rheumatoid arthritis, Sjögren's syndrome and systemic lupus erythematosus.

interpretationGut microbiota dysbiosis was associated with rheumatic diseases, principally with potentially non-specific, shared alterations of microbes.

fundingNational Natural Science Foundation of China (81930071, 81902265, 82072502 and U21A20352).

Indexed as

Gastrointestinal MicrobiomeLupus Erythematosus, SystemicRheumatic DiseasesSjogren's SyndromeDysbiosisHumansGut dysbiosisGut microbiotaMeta-analysisRheumatic diseases

Identifiers

PMID35594658
PMCPMC9120231
OpenAlexW4280553002

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.